Evidence map›Paper›PMID 25796440›Full record

ReviewCancer letters2015

Mechanisms regulating glioma invasion.

Ivy Paw, Richard C Carpenter, Kounosuke Watabe, Waldemar Debinski, Hui-Wen Lo

Abstract readReview
In one paragraph

Review in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed, 1 pooled it
19.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

186 citing papers in PubMed, 1 synthesis or guideline pooled it, 311 citations in OpenAlex.

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126 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Ivy PawDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Richard C CarpenterDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Kounosuke WatabeDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Brain Tumor Center of Excellence, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Waldemar DebinskiDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Brain Tumor Center of Excellence, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Hui-Wen LoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Brain Tumor Center of Excellence, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA; Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. Electronic address: hlo@wakehealth.edu.
Wake Forest University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Training Program in Cancer BiologyT32CA079448 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KRIDEL, STEVEN J. · 2000 to 2014
$6.5M
Truncated GLI1 In GlioblastomaR01NS087169 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LO, HUI-WEN · 2014 to 2018
$2.1M
NCI NIH HHS 5T32CA079448NCI NIH HHS P30 CA012197NCI NIH HHS P30CA012197NCI NIH HHS T32 CA079448NINDS NIH HHS 7R01NS087169-02NINDS NIH HHS R01 NS087169
6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive, deadliest, and most common brain malignancy in adults. Despite the advances made in surgical techniques, radiotherapy and chemotherapy, the median survival for GBM patients has remained at a mere 14 months. GBM poses several unique challenges to currently available treatments for the disease. For example, GBM cells have the propensity to aggressively infiltrate/invade into the normal brain tissues and along the vascular tracks, which prevents complete resection of all malignant cells and limits the effect of localized radiotherapy while sparing normal tissue. Although anti-angiogenic treatment exerts anti-edematic effect in GBM, unfortunately, tumors progress with acquired increased invasiveness. Therefore, it is an important task to gain a deeper understanding of the intrinsic and post-treatment invasive phenotypes of GBM in hopes that the gained knowledge would lead to novel GBM treatments that are more effective and less toxic. This review will give an overview of some of the signaling pathways that have been shown to positively and negatively regulate GBM invasion, including, the PI3K/Akt, Wnt, sonic hedgehog-GLI1, and microRNAs. The review will also discuss several approaches to cancer therapies potentially altering GBM invasiveness.

Indexed as

AnimalsBrain NeoplasmsGlioblastomaHumansNeoplasm InvasivenessGlioblastomaHedgehogInvasionPI3KWnt

Identifiers

PMID25796440
PMCPMC4435977
OpenAlexW2034437737

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.